阿霉素对SD大鼠心肌纤维化的影响机制  

Effect of adriamycin on myocardial fibrosis and possible mechanisms in rats

作　　者：暴云锋[1] 王晶晶[2] 诸葛铭宁[3] 张洪珍[2] 

机构地区：[1]河北省人民医院医学影像科,河北石家庄050051 [2]河北省人民医院肿瘤五科,河北石家庄050051 [3]河北省人民医院急诊科,河北石家庄050051

出　　处：《河北医科大学学报》2016年第3期252-255,共4页Journal of Hebei Medical University

摘　　要：目的探讨阿霉素对大鼠心肌纤维化的影响机制。方法尾静脉注射阿霉素6周(3mg/kg,每周1次),观察大鼠的一般情况及体质量,于第7周检测血流动力学指标、羟脯氨酸含量及心肌组织形态学的变化。结果与正常对照组比较,阿霉素模型组心肌组织中的羟脯氨酸含量升高,组织病理学进一步证实阿霉素对心肌纤维化的诱导作用,血流动力学检测显示左心室舒张末期压升高,左心室收缩压、左心室压最大上升速率及最大下降速率降低,差异有统计学意义(P<0.05)。结论阿霉素可以诱导大鼠心肌纤维化,抑制心功能。Objective To determine the effect of adriamycin on myocardial fibrosis and possible mechanisms in rats. Methods A rat myocardial fibrotic model was induced by intravenous injection of adriamycin（3 mg/kg,once a week）for six weeks.During the test,general condition and body weight were observed. At the seventh week,hemodynamic parameters and hydroxyproline concentration as well as morphological transformation of heart tissues were detected.Results Compared to those in control group,hydroxyproline content was markedly increased in adriamycin induced rats.Histopathological examination further confirmed the same alteration. Moreover,hemodynamics showed a significant decline in left-ventricular systolic pressure,maximum and minimum rate of developed left ventricular pressure,accompanied by an increment of left ventricular end-diastolic pressure（P〈0.05）.Conclusion These findings suggested that adriamycin could induce myocardial fibrosis and inhibit cardiac function.

关 键 词：心内膜心肌纤维化症 阿霉素 大鼠 

分 类 号：R542.23[医药卫生—心血管疾病]